Ventricular-Arterial Coupling in Chronic Heart Failure.
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ABSTRACT:
SUBMITTER: Chirinos JA
PROVIDER: S-EPMC5494149 | biostudies-other | 2017 Apr
REPOSITORIES: biostudies-other
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Project description:The objective of this study was to compare the physiological determinants of ejection fraction (EF)-ventricular size, contractile function, and ventricular-arterial (VA) interaction-and their associations with clinical outcomes in chronic heart failure (HF).EF is a potent predictor of HF outcomes, but represents a complex summary measure that integrates several components including left ventricular size, contractile function, and VA coupling. The relative importance of each of these parameters in determining prognosis is unknown.In 466 participants with chronic systolic HF, we derived quantitative echocardiographic measures of EF: cardiac size (end-diastolic volume [EDV]); contractile function (the end-systolic pressure volume relationship slope [Eessb] and intercept [V0]); and VA coupling (arterial elastance [Ea]/Eessb). We determined the association between these parameters and the following adverse outcomes: 1) the combined endpoint of death, cardiac transplantation, or ventricular assist device (VAD) placement; and 2) cardiac hospitalization.Over a median follow-up of 3.4 years, there were 76 deaths, 52 transplantations, 14 VAD placements, and 684 cardiac hospitalizations. EF was independently associated with death, transplantation, and VAD placement (adjusted hazard ratio [HR]: 3.0; 95% confidence interval [CI]: 1.8 to 5.0 comparing third and first tertiles), as were EDV (HR: 2.6; 95% CI: 1.5 to 4.2); V0 (HR: 3.6; 95% CI: 2.1 to 6.1); and Ea/Eessb (HR: 2.1; 95% CI: 1.3 to 3.3). EDV, V0, and Ea/Eessb were also associated with risk of cardiac hospitalization. Eessb was not significantly associated with any adverse outcomes in adjusted analyses.Left ventricular size, V0, and VA coupling are associated with prognosis in systolic HF, but end-systolic elastance (Eessb) is not. Assessment of VA coupling via Ea/Eessb is an additional noninvasively derived metric that can be used to gauge prognosis in human HF.
| S-EPMC3943424 | biostudies-literature
Project description:Left ventricular ejection fraction (LVEF) and ventricular-arterial coupling (VAC) [VAC = Ea/Ees; Ea: effective arterial elastance; Ees: left ventricle (LV) elastance] are both dimensionless ratios with important limitations, especially in heart failure setting. The LVEF to VAC relationship is a divergent non-linear function, having a point of intersection at the specific value of 0.62, where V0 = 0 ml (V0: the theoretical extrapolated value of the volume-axis intercept at end-systolic pressure 0 mmHg). For the dilated LV, both LVEF and VAC are highly dependent on V0 which is inconclusive when derived from single-beat Ees formulas. VAC simplification should be avoided. Revisiting the relationship between systolic time intervals (STI), pressure, and volumes could provide simple-to-use guiding formulas, affordable for daily clinical practice. We have analyzed by echocardiography the hemodynamics of 21 patients with severe symptomatic heart failure with reduced ejection (HFrEF) compared to 12 asymptomatic patients (at risk of heart failure with mild structural disease). The groups were unequivocally separated by 'classic' measures (LVEF, LV end-systolic volume (ESV), LV mass, STI). Chen's Ees formula was weakly correlated with LVEF and indexed ESV (ESVi) but better correlated to the pre-ejection period (PEP); PEP/total ejection time (PEP/TET); systolic blood pressure/PEP (SBP/PEP) (P < 0.001). Combining the predictability of the LVEF to the determinant role of SBP/PEP on the Ees variations, we obtained: (SBP*LVEF)/PEP mm Hg/ms, with an improved R 2 value (R 2 = 0.848; P < 0.001). The strongest correlations to VAC were for LVEF (R = -0.849; R 2 = 0.722) and PEP/TET (R = 0.925; R 2 = 0.857). By multiple regression, the VAC was strongly predicted (N = 33): (R = 0.975; R 2 = 0.95): VAC = 0.553-0.009*LVEF + 3.463*PEP/TET, and natural logarithm: Ln (VAC) = 0.147-1.4563*DBP/SBP*0.9-0.010*LVEF + 4.207*PEP/TET (R = 0.987; R 2 = 0.975; P = 0) demonstrating its exclusive determinants: LVEF, PEP/TET, and DBP/SBP. Considering Ea as a known value, the VAC-derived Ees formula: Ees_d ≈ Ea/(0.553-0.009*LVEF+3.463*PEP/TET) was strongly correlated to Chen's Ees formula (R = 0.973; R 2 = 0.947) being based on SBP, ESV, LVEF, and PEP/TET and no exponential power. Thus, the new index supports our hypothesis, in the limited sample of patients with HFrEF. Indices like SBP/PEP, (SBP*LVEF)/PEP, PEP/TET, and DBP/SBP deserve further experiments, underlining the major role of the forgotten STI.
| S-EPMC8813963 | biostudies-literature
Project description:BackgroundRight ventricular-pulmonary artery coupling (RVPAC) refers to the relationship between right ventricular systolic force and afterload. The ratio of echocardiograph-derived tricuspid annular plane systolic excursion (TAPSE) to pulmonary artery systolic pressure (PASP) has been proposed as a noninvasive measurement of RVPAC and reported as an independent prognostic parameter of heart failure. However, it has not been adequately in detail evaluated in heart failure with preserved ejection fraction (HFpEF). We hypothesized that RVPAC may be used and proposed as an expression of key risk factors in patients with HFpEF.MethodsWe retrospectively analyzed TAPSE/PASP of 648 HFpEF patients hospitalized in Chongqing Hospital of Traditional Chinese Medicine from January 1, 2016 to January 1, 2017. All eligible patients were followed up for 5 years. The correlation between TAPSE/SPAP index and clinical indicators and outcomes was evaluated.ResultsThe final analysis included 414 patients. Nonsurvivors had significantly lower TAPSE, TAPSE/PASP and higher PASP compared with survivors (p < 0.0001). ROC curve analysis showed that the optimal cutoff of TAPSE, PASP, and RVPAC to predict all-cause death were 16.5 mm, 37.5 mmHg, and 0.45 mm/mmHg, respectively. In multivariate Cox regression analyses adjusted for gender showed a significant, independent association of the RVPAC with the composite endpoint of all-cause death or HF-related recurrent hospitalization (HR: 0.006; 95% CI 0.001-0.057, p < 0.001).ConclusionsRVPAC, defined by the ratio of TAPSE to PASP, is the expression of a key risk factor in HFpEF patients, which is independently associated with the composite endpoint of all-cause death or HF-related recurrent hospitalization.
| S-EPMC11249816 | biostudies-literature
Project description:AimAcyl ghrelin increases cardiac output (CO) in heart failure with reduced ejection fraction (HFrEF). This could impair the right ventricular-pulmonary arterial coupling (RVPAC), both through an increased venous return and right ventricular afterload. We aim to investigate if acyl ghrelin increases CO with or without worsening the right-sided haemodynamics in HFrEF assessed by RVPAC.Methods and resultsThe Karolinska Acyl ghrelin Trial was a randomized double-blind placebo-controlled trial of acyl ghrelin versus placebo (120-min intravenous infusion) in HFrEF. RVPAC was assessed echocardiographically at baseline and 120 min. ANOVA was used for difference in change between acyl ghrelin versus placebo, adjusted for baseline values. Of the 30 randomized patients, 22 had available RVPAC (acyl ghrelin n = 12, placebo n = 10). Despite a 15% increase in CO in the acyl ghrelin group (from 4.0 (3.5-4.6) to 4.6 (3.9-6.1) L/min, P = 0.003), RVPAC remained unchanged; 5.9 (5.3-7.6) to 6.3 (4.8-7.5) mm·(m/s)-1 , P = 0.372, while RVPAC was reduced in the placebo group, 5.2 (4.3-6.4) to 4.8 (4.2-5.8) mm·(m/s)-1 , P = 0.035. Comparing change between groups, CO increased in the acyl ghrelin group versus placebo (P = 0.036) while RVPAC and the right ventricular pressure gradient remained unchanged.ConclusionTreatment with acyl ghrelin increases CO while preserving or even improving RVPAC in HFrEF, possibly due to increased contractility, reduced PVR and/or reduced left sided filling pressures. These potential effects strengthen the role of acyl ghrelin therapy in HFrEF with right ventricular failure.
| S-EPMC10804189 | biostudies-literature
Project description:Apelin plays important roles in cardiovascular homeostasis. However, its effects on the mechanoenergetics of heart failure (HF) are unavailable. We attempted to investigate the effects of apelin on the left ventricular-arterial coupling (VAC) and mechanical efficiency in rats with HF. HF was induced in rats by the ligation of the left coronary artery. The ischemic HF rats were treated with apelin or saline for 12 weeks. The sham-operated animals served as the control. The left ventricular (LV) afterload and the systolic and diastolic functions, as well as the mechanoenergetic indices were estimated from the pressure-volume loops. Myocardial fibrosis by Masson's trichrome staining, myocardial apoptosis by TUNEL, and collagen content in the aorta as well as media area in the aorta and the mesenteric arteries were determined. Our data indicated that HF rats manifested an increased arterial load (Ea), a declined systolic function (reduced ejection fraction, +dP/dtmax, end-systolic elastance, and stroke work), an abnormal diastolic function (elevated end-diastolic pressure, ?, and declined -dP/dtmax), and decreased mechanical efficiency. Apelin treatment improved those indices. Concomitantly, increased fibrosis in the LV myocardium and the aorta and enhanced apoptosis in the LV were partially restored by apelin treatment. A declined wall-to-lumen ratio in the mesenteric arteries of the untreated HF rats was further reduced in the apelin-treated group. We concluded that the rats with ischemic HF were characterized by deteriorated LV mechanoenergetics. Apelin improved mechanical efficiency, at least in part, due to the inhibiting cardiac fibrosis and apoptosis in the LV myocardium, reducing collagen deposition in the aorta and dilating the resistant artery.
| S-EPMC6604493 | biostudies-literature
Project description:The echocardiographic tricuspid annular plane systolic excursion/pulmonary artery systolic pressure (TAPSE/PASP) ratio is a non-invasive surrogate of right ventricular-pulmonary arterial (RV-PA) coupling which corresponds well with the respective invasively derived index. Recently, a wealth of observational data has arisen, outlining its prognostic value in heart failure (HF) patients. To systematically appraise and quantitatively synthesize the evidence of the prognostic value of TAPSE/PASP ratio in left-sided HF regardless of etiology or left ventricular ejection fraction. A systematic literature review was conducted in electronic databases to identify studies reporting the association of TAPSE/PASP ratio with outcomes in patients with HF and, when appropriate, a random-effects meta-analysis was conducted to quantify the unadjusted and adjusted hazard ratios [(a)HRs] for all-cause death and the composite outcome of all-cause death or HF hospitalization. Eighteen studies were deemed eligible encompassing 8,699 HF patients. The applied cut-off value for RV-PA uncoupling varied substantially from 0.27 to 0.58 mm/mmHg, and in most studies values lower than the applied cutoff conveyed dismal prognosis. Eleven studies reported appropriate data for meta-analysis. TAPSE/PASP reduction by 1 mm/mmHg was independently associated with all-cause death (pooled aHR=1.32 [1.06-1.65]; p=0.01; I2=56%) and the composite outcome (pooled aHR=3.48 [1.67-7.25]; p<0.001; I2=0%). When a TAPSE/PASP cutoff value of 0.36 mm/mmHg was applied it yielded independent association with all-cause death (pooled aHR=2.84 [2.22-3.64]; p<0.001; I2=82%). RV-PA coupling assessed by echocardiographic TAPSE/PASP ratio appears to be an independent outcome predictor for HF patients.
| S-EPMC10904417 | biostudies-literature
Project description:Heart failure with preserved ejection fraction (HFPEF) involves failure of cardiovascular reserve in multiple domains. In HFPEF animal models, dietary sodium restriction improves ventricular and vascular stiffness and function. We hypothesized that the sodium-restricted dietary approaches to stop hypertension diet (DASH/SRD) would improve left ventricular diastolic function, arterial elastance, and ventricular-arterial coupling in hypertensive HFPEF.Thirteen patients with treated hypertension and compensated HFPEF consumed the DASH/SRD (target sodium, 50 mmol/2100 kcal) for 21 days. We measured baseline and post-DASH/SRD brachial and central blood pressure (via radial arterial tonometry) and cardiovascular function with echocardiographic measures (all previously invasively validated). Diastolic function was quantified via the parametrized diastolic filling formalism that yields relaxation/viscoelastic (c) and passive/stiffness (k) constants through the analysis of Doppler mitral inflow velocity (E-wave) contours. Effective arterial elastance (Ea) end-systolic elastance (Ees) and ventricular-arterial coupling (defined as the ratio Ees:Ea) were determined using previously published techniques. Wilcoxon matched-pairs signed-rank tests were used for pre-post comparisons. The DASH/SRD reduced clinic and 24-hour brachial systolic pressure (155 ± 35 to 138 ± 30 and 130 ± 16 to 123 ± 18 mm Hg; both P=0.02), and central end-systolic pressure trended lower (116 ± 18 to 111 ± 16 mm Hg; P=0.12). In conjunction, diastolic function improved (c=24.3 ± 5.3 to 22.7 ± 8.1 g/s; P=0.03; k=252 ± 115 to 170 ± 37 g/s(2); P=0.03), Ea decreased (2.0 ± 0.4 to 1.7 ± 0.4 mm Hg/mL; P=0.007), and ventricular-arterial coupling improved (Ees:Ea=1.5 ± 0.3 to 1.7 ± 0.4; P=0.04).In patients with hypertensive HFPEF, the sodium-restricted DASH diet was associated with favorable changes in ventricular diastolic function, arterial elastance, and ventricular-arterial coupling.URL: http://www.clinicaltrials.gov. Unique identifier: NCT00939640.
| S-EPMC4017662 | biostudies-literature
Project description:AimTo evaluate the long-term prognostic significance of right ventricular (RV) deformation and RV-arterial coupling in a cohort of patients with heart failure (HF) due to severe aortic stenosis (AS) candidate for trans-catheter aortic valve implantation (TAVI).MethodsThe study is a retrospective analysis of 56 patients undergoing echocardiography before TAVI execution. RV function was defined by tricuspid annular plane systolic excursion (TAPSE), fractional area change (FAC), peak systolic myocardial velocity by tissue Doppler imaging (RVSm) and RV longitudinal strain (RVLS). RV-arterial coupling were defined as TAPSE and RVLS normalized for systolic pulmonary artery pressure (sPAP) to obtain afterload-independent parameters: TAPSE/sPAP and RVLS/sPAP, respectively. All-cause mortality was the primary endpoint of survival analysis; composite of death and hospitalization for HF was the secondary endpoint.ResultsAll patients underwent TAVI from femoral access. Mean age was 81.6±6.3 years and left ventricular ejection fraction was preserved in most patients (51±15%). At 10 years, using Cox regression analysis adjusted for the parameters related to prognosis at univariate analysis, we found that only pre-procedural RVLS was independently associated with all-cause mortality (aHR 1.53, 95% CI 1.10-2.12, P=0.011). RVLS (aHR 7.542, 95% CI 1.325-42.921, P=0.023), sPAP (aHR 1.421, 95% CI 1.045-1.932, P=0.025), TAPSE/sPAP (aHR 4.977, 95% CI 5.425-21.99, P=0.044) and RVLS/sPAP (aHR 2.333, 95% CI 3.9677-12.999, P=0.046) were independently associated with the secondary endpoint.ConclusionsAmong patients with HF due to severe AS undergoing TAVI, deformation imaging (i.e., RVLS) and RV-arterial coupling (i.e., TAPSE/sPAP and RVLS/sPAP) provide better risk stratification at long-term follow up of 10 years than other RV echocardiographic parameters.
| S-EPMC7486529 | biostudies-literature
Project description: Not available
| S-EPMC9314840 | biostudies-literature
Project description:Excitation-contraction (EC) coupling is altered in end-stage heart failure. However, spatial heterogeneity of this remodeling has not been established at the tissue level in failing human heart. The objective of this article was to study functional remodeling of excitation-contraction coupling and calcium handling in failing and nonfailing human hearts.We simultaneously optically mapped action potentials and calcium transients in coronary perfused left ventricular wedge preparations from nonfailing (n=6) and failing (n=5) human hearts. Our major findings are the following. First, calcium transient duration minus action potential duration was longer at subendocardium in failing compared with nonfailing hearts during bradycardia (40 bpm). Second, the transmural gradient of calcium transient duration was significantly smaller in failing hearts compared with nonfailing hearts at fast pacing rates (100 bpm). Third, calcium transient in failing hearts had a flattened plateau at the midmyocardium and exhibited a 2-component slow rise at the subendocardium in 3 failing hearts. Fourth, calcium transient relaxation was slower at the subendocardium than at the subepicardium in both groups. Protein expression of sarcoplasmic reticulum Ca(2+)-ATPase 2a was lower at the subendocardium than the subepicardium in both nonfailing and failing hearts. Sarcoplasmic reticulum Ca(2+)-ATPase 2a protein expression at subendocardium was lower in hearts with ischemic cardiomyopathy compared with those with nonischemic cardiomyopathy.For the first time, we present direct experimental evidence of transmural heterogeneity of excitation-contraction coupling and calcium handling in human hearts. End-stage heart failure is associated with the heterogeneous remodeling of excitation-contraction coupling and calcium handling.
| S-EPMC3100201 | biostudies-literature